Arachidonic acid fuels inflammation by unlocking macrophage protein phosphatase 5 after myocardial infarction
Authors' conclusion
The findings elucidate the conserved role of 5-lipoxygenase phosphorylation regulated LTB4 levels in MI and identify PP5 as a potential therapeutic target for the treatment of MI.
Study context
- Population
- Myocardial infarction (MI) patients and post-MI mice
Methodological detailsSingle-cell RNA-seq of cardiac macrophages in post-MI mice; metabolomics of PUFA metabolites in MI patients' plasma and infarcted mouse hearts
- Single-cell RNA-seq of cardiac macrophages in post-MI mice; metabolomics of PUFA metabolites in MI patients' plasma and infarcted mouse hearts
Main finding
As reported in the abstract
- Leukotriene B4 (LTB4) consistently elevated in MI patients and mouse models; significantly higher plasma levels in recurrent MI
- Arachidonic acid (AA) promotes nuclear translocation of PP5, which dephosphorylates 5-lipoxygenase at Thr218, driving sustained LTB4 production
- Enhanced CXCL13-mediated B-cell recruitment; inflammation amplified via macrophage-B-cell crosstalk
- Disruption of PP5 in mouse macrophages prevents these adverse changes
Original publication
Arachidonic acid fuels inflammation by unlocking macrophage protein phosphatase 5 after myocardial infarction. Eur Heart J. Published 4 September 2025. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →